Anxiety disorders are among the most common mental disorders in America, affecting 40 million adults (Anxiety and Depression Association of America [ADAA], n.d.). The disorder describes several sub-types, such as Generalized Anxiety Disorder (GAD), Obsessive-Compulsive Disorder (OCD), Post-Traumatic Stress Disorder (PTSD), Social Anxiety Disorder (SAD), and Panic Disorder (PD). Of those subsets, GAD is the most common, occurring in 6.8 million adults, most of whom are women, or 3.1% of the population (ADAA, n.d.). Because of its common occurrence, this paper will focus on GAD.
The exact cause of anxiety disorders is unknown. Studies suggest that there is a biological factor that takes place in the brain, such as low levels of Gamma-Aminobutyric Acid (GABA) contributing to hyperactivity in the central nervous system, and common chemicals such as serotonin (ScienceDaily, 2008). There is, however, a strong push against the chemical imbalance theory, which they claim is a marketing ploy created by pharmaceutical companies to sell drugs they deem largely unnecessary, instead emphasizing the importance of situational factors, such as early childhood trauma (Sanua, 1996).
Watson, Clark, and Carey (1988) found that general disposition, or Positive and Negative Affect, can affect how anxiety disorders manifest in patients. The study defines these effects as “a broad and pervasive predisposition to experience negative emotions,” and “one’s level of pleasurable engagement with the environment” (Watson et al., 1988). The results of the study emphasize how much influence situational factors do have on a patient’s mental health, allowing them to succumb to or manage their disorder more easily.
However, the efficacy of Selective Serotonin Reuptake Inhibitors (SSRIs) tend to lend credence to the idea that chemical imbalance does play a role in the causes of anxiety disorders; 60-70% of patients managing their GAD with SSRIs in clinical trials responded to treatment, which shows that while not universally effective, SSRIs have a large pool of efficacy in helping patients manage their disorder (Springer International Publishing).
Heim and Memeroff (1999) discuss the effect of early trauma and events in the role of developing anxiety disorders. Heim and Memeroff (1999) state that women who faced abuse in childhood were four times more likely to develop a mood disorder, including both chronic depression and anxiety disorders; they also admit a likely connection between genetic predispositions and the triggering trauma, which gives some credibility to the idea of a brain-based source for the disorder, whether it is chemically induced or related to functions within the brain, like the amygdala or neurotransmitters.
Evidence exists for the involvement of the amygdala, the area of the brain responsible for controlling fear response, which shows disconnects from other portions of the brain that interpret stimuli, and denser grey matter which impedes communication between the amygdala and portions of the brain such as the brainstem, hypothalamus, and cerebellum (Etkin, 2009). Furthermore, during MRI screenings, patients with SAD were shown images of aggressive or angry faces, showing that the patient’s amygdala was hyper-reactive, stimulating an exaggerated fear response (Evans, Wright, Wedig, Gold, Pollack, & Rauch, 2008).
GAD can become a very physically taxing disorder when paired with panic attacks, as the National Institute of Mental Health (NIMH) reports is very common (NIHM, 2009); panic attacks can stimulate the same reactions in a fight-or-flight situation, increasing heart rate, a sense of impending danger, trembling, dizziness, weakness in the limbs, chest pain, difficulty breathing or the sensation of being smothered, nausea, faintness, chill, or overheating (NIHM, 2009).
On its own, GAD has physical, mental, and social ramifications, including irrational and unrealistic worries about specific outcomes to situations, and avoidance and procrastination (Gliatto, 2000). GAD is connected to other physical illnesses or ailments, including irritable bowel syndrome (IBS), pulmonary disease, and diabetes, and often leads to poorer health and higher rates of substance abuse than non-anxious patients (Gliatto, 2000).
The diagnostic criteria according to the Diagnostic and Statistical Manual, 4th ed. (DSM-IV; 1994) for GAD must be met more often than not for a time period of six months, must negatively affect the patient’s life, and aside from difficulty in controlling excessive worry or anxiety, must include at least three of the following: Restlessness or feeling on edge; Being easily fatigued; Difficulty concentrating; Irritability; Muscle-tension; Sleep disturbance, either difficulty falling asleep and staying asleep, or restless sleep.
To evaluate a patient for GAD, the attending clinician must do the following: Evaluate for a medical condition; Evaluate use of over-the-counter or herbal medications for side effects; Assess for any substance abuse, including caffeine and nicotine, as well as prescription drugs; Assess social stressors that may have triggered the anxiety; Evaluate for the criteria mentioned above; Remove abused substances; Assess for related disorders, such as major depression and panic disorders (Gliatto, 2000).
Acute anxiety is categorized as being more low-level or less intense than panic attacks, which last only for a few minutes; a period of anxiety for someone with GAD can last anywhere from a few hours to weeks if they are triggered by a powerful stressor (Gliatto, 2000). Additionally, not all patients experience the same symptoms, and not all at the same intensities, making it important to closely assess the reported symptoms for underlying causes and family history, to better understand the diagnosis.
The most common treatments for GAD are cognitive-behavioral therapy (CBT) and antidepressant or antianxiety medication. Medication is used most often in tandem with psychotherapy, allowing the patient to manage their symptoms more effectively, while the CBT works on treating the underlying issues that lead to the anxiety, which ultimately can lead to the patient having a normal life in which his or her disorder no longer negatively affects their ability to maintain responsibilities to work or school and other obligations (NIHM, 2009).
The most common antidepressants used to treat anxiety disorders are SSRIs, which alter the levels of serotonin in the brain, allowing previously disconnected portions of the brain to communicate (NIHM, 2009). Anti-anxiety medication such as Xanax or Clonazepam is often used only in short-term cases, as they can cause dependency, especially in patients with a history of addiction or substance abuse, and can have harsh withdrawal symptoms if not tapered off (NIHM, 2009).
Psychotherapy is used without medication for patients with mild disorders, but more severe cases often require both treatments at once; cognitive therapy helps a patient to recognize harmful patterns of thought and unrealistic fears to better understand and manage the thought patterns that lead to anxiousness (Gliatto, 2000). It tends to focus on relaxation techniques to soothe symptoms, and manage them outside of therapeutic situations, and about finding more effective ways to deal with avoidance and procrastination frequently associated with GAD (Gliatto, 2000; Fricchione, 2004). Family members are helpful resources in the therapeutic stage, as they offer support in recognizing anxious thought patterns, problem-solving, and encouragement in facing anxiety triggers in a safe manner, allowing the patient to desensitize themselves and manage their symptoms (Gliatto, 2000).
One study found that in three months, 32% of patients in CBT sessions had significant improvements, and in six months, 42% had significant improvements, while the control group saw no significant improvement (Fricchione, 2004). Relaxation therapy, which has a similar rate of success, is the second form of CBT (Fricchione, 2004).
Patients with more severe forms of GAD should attend psychotherapy every two to four weeks, but may taper that amount during the maintenance phase of treatment; medication should be taken for no longer than one year, then tapered off (Fricchione, 2004).
Group therapy or finding other patients with anxiety disorders, even on the Internet, can be useful for helping a patient to find therapeutic methods for managing their disorder, by sharing experiences and understanding that they are not alone, receiving support for personal achievements that may not be understood by non-anxious people, especially with a wide-spread stigma against mental health still common in America (Ben-Zeev, Young, & Corrigan, 2010; NIMH, 2009). Aerobic exercise such as yoga has been the subject of recent studies to discover whether it has beneficial effects, but eliminating substances such as caffeine, nicotine, and alcohol is known to assist in symptom management (NIHM, 2009).
GAD is rarely present on its own but is instead paired frequently with panic disorders, or more frequently, in about two-thirds of patients, with major depression (Gilatto, 2000; Fricchione, 2004). Some professionals argue that GAD is only a subset or variant of panic disorder or major depression because its symptoms and causes overlap with other disorders, and thus it is only diagnosed after the exclusion of every other disorder (Gliatto, 2000).
References
Ben-Zeev, D., Young, M. A., & Corrigan, P. W. (2010). DSM-V and the stigma of mental illness. Journal of Mental Health, 19(4), 318-327.
Diagnostic and statistical manual of mental disorders: DSM-IV. (4th ed.). (1994). Washington, DC: American Psychiatric Association.
Enna, S.J. (1984). Role of gamma-aminobutyric acid in anxiety. Psychopathology, 17(1), 15–24.
Etkin A., Prater K.E., Schatzberg A.F., Menon V., Greicius M.D. (2009). "Disrupted amygdalar subregion functional connectivity and evidence of a compensatory network in generalized anxiety disorder." Archives of General Psychiatry 66(12): 1361–1372.
Evans, K. C., Wright, C. I., Wedig, M. M., Gold, A. L., Pollack, M. H., & Rauch, S. L. (2008). A functional MRI study of amygdala responses to angry schematic faces in social anxiety disorder. Depression and Anxiety, 25(6), 496-505.
Fricchione, G. (2004). Generalized anxiety disorder. New England Journal of Medicine, 351(7), 675-682.
Gliatto, M. F. (2000). Generalized anxiety disorder. American Family Physician, 62(7), 1591-1600.
Heim, C., & Nemeroff, C. B. (1999). The impact of early adverse experiences on brain systems involved in the pathophysiology of anxiety and affective disorders. Biological Psychiatry, 46(11), 1509-1522.
National Institute of Mental Health. (2009). Anxiety disorders. NIH Publication No. 09 3879.
PLoS Computational Biology. (2008). Why serotonin can cause depression and anxiety. ScienceDaily.
Sanua, V. D. (1996). The myth of the organicity of mental disorders. The Humanistic Psychologist, 24(1), 55-78.
Springer International Publishing. (2010). Antidepressants are the main options for the long-term pharmacological treatment of generalized anxiety disorder. Drugs & Therapy Perspectives, 26(1), 12-15.
Watson, D., Clark, L. A., & Carey, G. (1988). Positive and negative affectivity and their relation to anxiety and depressive disorders. Journal of Abnormal Psychology, 97(3), 346-353.
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